M A Hege1, K T Stingl2, S Kullmann3, K Schag4, K E Giel4, S Zipfel4, H Preissl3. 1. 1] Institute of Medical Psychology and Behavioural Neurobiology/fMEG Center, University Tübingen, Tübingen, Germany [2] Graduate School of Neural and Behavioural Sciences, International Max Planck Research School, University Tübingen, Tübingen, Germany. 2. 1] Institute of Medical Psychology and Behavioural Neurobiology/fMEG Center, University Tübingen, Tübingen, Germany [2] Department of Neonatology, University Children's Hospital Tübingen, Tübingen, Germany. 3. 1] Institute of Medical Psychology and Behavioural Neurobiology/fMEG Center, University Tübingen, Tübingen, Germany [2] German Center for Diabetes Research (DZD), Neuherberg, Germany [3] Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen (IDM), Tübingen, Germany. 4. Department of Psychosomatic Medicine and Psychotherapy, Medical University Hospital Tübingen, Tübingen, Germany.
Abstract
BACKGROUND: A subgroup of overweight and obese people is characterized by binge eating disorder (BED). Increased impulsivity has been suggested to cause binge eating and subsequent weight gain. In the current study, neuronal correlates of increased impulsivity in binge eating disorder during behavioral response inhibition were investigated. METHODS: Magnetic brain activity and behavioral responses of 37 overweight and obese individuals with and without diagnosed BED were recorded while performing a food-related visual go-nogo task. Trait impulsivity was assessed with the Barratt Impulsiveness Scale (BIS-11). RESULTS: Specifically, increased attentional impulsiveness (a subscale of the BIS-11) in BED was related to decreased response inhibition performance and hypoactivity in the prefrontal control network, which was activated when response inhibition was required. Furthermore, participants with BED showed a trend for a food-specific inhibition performance decline. This was possibly related to the absence of a food-specific activity increase in the prefrontal control network in BED, as observed in the control group. In addition, an increase in activity related to the actual button press during prepotent responses and alterations in visual processing were observed. CONCLUSIONS: Our results suggest an attentional impulsiveness-related attenuation in response inhibition performance in individuals with BED. This might have been related to increased reward responsiveness and limited resources to activate the prefrontal control network involved in response inhibition. Our results substantiate the importance of neuronal markers for investigating prevention and treatment of obesity, especially in specific subgroups at risk such as BED.
BACKGROUND: A subgroup of overweight and obesepeople is characterized by binge eating disorder (BED). Increased impulsivity has been suggested to cause binge eating and subsequent weight gain. In the current study, neuronal correlates of increased impulsivity in binge eating disorder during behavioral response inhibition were investigated. METHODS: Magnetic brain activity and behavioral responses of 37 overweight and obese individuals with and without diagnosed BED were recorded while performing a food-related visual go-nogo task. Trait impulsivity was assessed with the Barratt Impulsiveness Scale (BIS-11). RESULTS: Specifically, increased attentional impulsiveness (a subscale of the BIS-11) in BED was related to decreased response inhibition performance and hypoactivity in the prefrontal control network, which was activated when response inhibition was required. Furthermore, participants with BED showed a trend for a food-specific inhibition performance decline. This was possibly related to the absence of a food-specific activity increase in the prefrontal control network in BED, as observed in the control group. In addition, an increase in activity related to the actual button press during prepotent responses and alterations in visual processing were observed. CONCLUSIONS: Our results suggest an attentional impulsiveness-related attenuation in response inhibition performance in individuals with BED. This might have been related to increased reward responsiveness and limited resources to activate the prefrontal control network involved in response inhibition. Our results substantiate the importance of neuronal markers for investigating prevention and treatment of obesity, especially in specific subgroups at risk such as BED.
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